Cocaine abuse has become a major public health problem in the United States, with over 20 million abusers in 1989. The quantity and frequency of cocaine use is increased markedly in the "recreational" cocaine user who switches to the high-intensity routes of cocaine administration, such as intravenous or free-base smoking. This high-intensity transition may lead to neurochemical and functional changes in the brain (Kosten (1989) J. Nervous and Mental Disease 177: 379-389). There is, therefore, presently an urgent need for improved methods of treatment for drug abuse involving cocaine. In addition to purely psychological treatments for helping cocaine abusers, there is a need for pharmacological treatments, especially for severe intravenous and free-base cocaine abusers.
Cocaine is reported to exert at least some of its pharmacological effects via the dopaminergic system. Chronic cocaine use in animals induces changes and increased sensitivity in postsynaptic dopaminergic receptors (Kosten (1989) J. Nervous and Mental Disease 177: 379-389).
Neuroleptic drugs, which are the primary antipsychotic drugs used in the treatment of schizophrenia, have been suggested for pharmacotherapy to treat psychotic symptoms during the early phase of withdrawal and recovery from cocaine abuse (Kosten (1989) J. Nervous and Mental Disease 177: 379-389). Such neuroleptics exert their therapeutic effects by binding to and blocking dopamine receptors, primarily D.sub.2 receptors (Snyder and Largent (1989) J. Neuropsychiatry 1: 7-15). Some neuroleptics, such as cinuperone, tiospirone, and haloperidol, are known to nonselectively antagonize both sigma and dopamine D.sub.2 receptors (Snyder and Largent (1989) J. Neuropsychiatry 1: 7-15).